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Acute glomerulonephritis

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Acute glomerulonephritis

  1. 1. Acute Glomerulonephritis Deepak Kumar Gupta Institute of Dental Education and Advance Studies, Gwalior
  2. 2. Glomerulonephritis • Inflammation of glomeruli • Mainly Immunologically mediated • Classification of GN is based on histopathological appearance. • Early investigation other than histological examination is very difficult
  3. 3. Etiology • Infectious diseases – Poststreptococcal glomerulnephritis – Infective endocaridtis – Syphilis – Viral – Mumps, measeles, hepatitis-b, c, inffectious mononucleosis, Epstein Barr Virus (EPV), – Malaria
  4. 4. Etiology • Collagen Vasculitis disorder – Systemic lupus erythematosus (SLE) – Good pasture’s syndrome – Henoch-schonlein purpura – Polyangitis – Wegner’s granulomatosis – Sickle cell nephropathy
  5. 5. Etiology • Primary glomerular disease – Focal segmental glomerulonephritis – Minimal change disorder – Rapidly progressive GN - Crescentric glomerulonephritis – Membranous glomerulonepritis – IgG nephropathy – Membranoproliferative GN – Mesengial proiliferative - IgA nephropathy – Meseangio-capillary glomerulonephritis
  6. 6. Etiology • Miscellaneous – Malignancy – Eclampsia (A toxic condition characterized by convulsions and possibly coma during or immediately after pregnancy) – Penicillamine
  7. 7. Pathogenesis • Two chief pathogenesis are recognised: – Deposition of anitgen-antibody complexes in glomeruli – Deposiotion of an antibody in glomerular basement membrane which then reacts with antigen in the basement membrane
  8. 8. Pathogenesis • Immune complexes are removed through hosts reticuloendothelial system – Impaired ability of the same results in deposition in glomerular capillary walls • Immune complex and antibody against glomerular antigen trigger injury by following mechanism • Complement activation • Fibrin deposition • Platelet aggregation • Release of cytokines and free oxygen radical
  9. 9. Clinical features • Haematuria • Hypertension • Red blood cell casts • Proteinuria • Oliguria • Oedema – areas of low tissue pressure (periorbital areas), but progresses to involve dependent portion of the body – May lead to ascitis or pleural effusion • Uraemia • pyuria
  10. 10. Management • Investigation – Urine microscopy – Red cell cast – Culture – throat swab α-beta hemolytic streptococci in case of of poststreptoccal infection – Antistreptolysin – O (ASO titre) – eleveated – C3 Level – reduced – Urinary protein – increased – Urea & creatinine – may be eleveated – Renal biopsy – features of glomerulnepritis
  11. 11. Treatment • Mainly supportive – Rest – Salt restriction – Diuretics – Anti-hypertensives – Antibiotics – in case of streptococcal infection – Dialysis – severe oliguria, fluid overload, hyperkalemia
  12. 12. Complications • Pulmonary edema • Hypertensive encephalopathy • Renal failure
  13. 13. Prognosis • Excellent in children • Small number of adult develops persistant hypertension or renal impairment later in life.
  14. 14. Poststreptococcal gomerulonephritis • Most common cause of GN • PSGN occurs fater pharyngeal or cutaneous attack with group A beta hemolytic streptococcus • Latent period of infection – Pharyngeal – 6-10 days – Cutaneous – 2 weeks – Commonly associated with poor hygiene, overcrowding & skin disease like scabies
  15. 15. Poststreptococcal gomerulonephritis • Onset abrupt with – Puffness of face – Oliguria – Smoky urine – Reddish urine – Hypertension – Oedema
  16. 16. Feel free to contact and give your valuable comments Facebook.com/dr.deepakkgupta Twitter.com/drdkg Dr.dkg07@gmail.com

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